The leukotrienes are a family of hydroxylated and peptide containing arachidonic acid metabolites that are thought to function as important mediators in the development and maintenance of spasmogenic, allergic IgE associated hypersensitivity, and inflammatory reactions. Within the last two years, reports in the literature have documented the occurrence of high quantities of leukotrienes in brain tissue following periods of ischemia and reperfusion. When injected into the peripheral vasculature, leukotrienes have been shown to decrease blood flow to the lungs, heart, and other organ systems via their potent vasoconstrictor capabilities. These observations indicate the potential association of leukotrienes with the occurrence of impaired blood flow, which in the brain may elicite mild to severe ischemia, stroke, and possibly even be associated with various progressive neurodegenerative disorders such as Parkinsonism or Huntington's Chorea. We propose on indepth study of leukotriene C4 (LTC4)-induced neurological dysfunction in cats. Leukotriene C, is of significant interest because it is primarily spasmogenic and not chemotactic (as is LTB4). In addition, LTC4 has been shown to be released from eosinophils, which are cells that circulate through the cerebral vasculature and have the capabilitiy to induce localized vasospasm and ischemia via the release of vasoconstrictive substances. Leukotriene C4-induced neurological dysfunction in cats will be initiated via unilateral infusion of LTC4 into left carotid aretery. Neurological dysfunction will be evaluated by analysis of time- and dose-response relationships of cerebral and retinal blood flow, EEG patterns, brainstem auditory evoked potentials (BAER), and neurological examinations, before, immediately after, and at 1, 3, 5, and 7 days after LTC4 infusion. Bilateral cerebral blood flow will be analyzed via the H2, perfusion technique. Leukotriene C4-induced changes in brain wave patterns will be assessed by recordings from 5 EEG electrodes places symmetrically on the head of each cat. Bilateral retinal blood perfusion will be ascertained via retinal photography at the given time periods. Bilateral alterations in the BAER due to LTC4 infusion will be recorded in response to an auditory stimuli. In addition, histological examination at the light microscope level will be performed on each brain and retina 7 days after leukotriene infusion. We believe that such a comprehensive evaluation of the pathophysiological role that leukotrienes may have in relation to the development of functional brain abnormalities will have clinical implications for the use of leukotriene antagonists in the treatment of neurological disease.